Role of vagal feedback from the lung in hypoxic-induced tachycardia in humans

Simon, Peggy M.; Taha, Basel; Dempsey, Jerome A.; Skatrud, James B.; Iber, Conrad

doi:10.1152/jappl.1995.78.4.1522

Cited by 26 publications

(27 citation statements)

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“…The increase in heart rate of humans in response to progressive IC systemic hypoxia has been shown to be linearly related to progressive arterial desaturation over a range of saturation from 100% to 70% (Sanders & Keller, 1989). Changes in mean heart rate normalised to percentage change in Sa.Oµ were found in this investigation to be of similar magnitude for both the supine and upright positions, and consistent with the range of values previously reported in the literature for healthy adult humans (Sanders & Keller, 1989;Simon et al 1995). These results suggest that in humans, unlike anaesthetised animals, the nature of the heart rate response to hypoxic stress is not critically dependent upon the pre-existing resting sympathovagal balance.…”

Section: Ic Hypoxia and Cardiac Sns Controlsupporting

confidence: 92%

Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

et al. 2000

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Neural mediation of the human cardiac response to isocapnic (IC) steady-state hypoxaemia was investigated using coarse-graining spectral analysis of heart rate variability (HRV). Six young adults were exposed in random order to a hypoxia or control protocol, in supine and sitting postures, while end-tidal PCOµ (PET,COµ) was clamped at resting eucapnic levels. An initial 11 min period of euoxia ( PET,Oµ 100 mmHg; 13.3 kPa) was followed by a 22 min exposure to hypoxia ( PET,Oµ 55 mmHg; 7.3 kPa), or continued euoxia (control). Harmonic and fractal powers of HRV were determined for the terminal 400 heart beats in each time period. Ventilation was stimulated (P < 0.05) and cardiac dynamics altered only by exposure to hypoxia. The cardiac interpulse interval was shortened (P < 0.001) similarly during hypoxia in both body positions. Vagally mediated highfrequency harmonic power (Ph) of HRV was decreased by hypoxia only in the supine position, while the fractal dimension, also linked to cardiac vagal control, was decreased in the sitting position (P < 0.05). However, lowfrequency harmonic power (Pl) and the HRV indicator of sympathetic activity (PlÏPh) were not altered by hypoxia in either position. These results suggest that, in humans, tachycardia induced by moderate IC hypoxaemia (arterial Oµ saturation Sa,Oµ 85 %) was mediated by vagal withdrawal, irrespective of body position and resting autonomic balance, while associated changes in HRV were positionally dependent .

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Section: Ic Hypoxia and Cardiac Sns Controlsupporting

confidence: 92%

Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

et al. 2000

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“…Other reports argue against a role of hyperpnoea in mediating the tachycardic effect of hypoxia in humans. No correlation between HR and ventilatory response to hypoxia was found in most studies in healthy subjects (Simon et al., ; Slutsky & Rebuck, ). Lung‐transplant patients with lung denervation displayed normal or reduced tachycardia (and never bradycardia) during systemic hypoxia in the study by Simon et al.…”

Section: Discussionmentioning

confidence: 91%

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Paleczny

Seredyński

Tubek

et al. 2019

Experimental Physiology

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New Findings What is the central question of this research?Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance?Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Abstract Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SnormalpO2)], tidal volume [Hyp‐VT; in litres per SnormalpO2], heart rate [Hyp‐HR; in beats per minute per SnormalpO2], systolic [Hyp‐SBP; in millimetres of mercury per SnormalpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SnormalpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SnormalpO2] was calculated as the slope of the regression line relating the variable to SnormalpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.

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“…A novel finding of this study, using dynamic time-varying analysis of HRV, was that short-term CIH selectively enhanced the maximum LF/HF values over time during acute hypoxia challenges. It is known that repetitive hypoxic episodes induce hyperventilation, increasing stroke volume, producing tachycardia (49), and sympathetic activation (22,44). Present data do not allow us to ascertain the underlying mechanisms of the LF/HF changes hereby described.…”

Section: Discussionmentioning

confidence: 99%

Dynamic time-varying analysis of heart rate and blood pressure variability in cats exposed to short-term chronic intermittent hypoxia

Rey¹,

Tarvainen²,

Karjalainen³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Rey S, Tarvainen MP, Karjalainen PA, Iturriaga R. Dynamic time-varying analysis of heart rate and blood pressure variability in cats exposed to short-term chronic intermittent hypoxia. Am J Physiol Regul Integr Comp Physiol 295: R28 -R37, 2008. First published May 7, 2008 doi:10.1152/ajpregu.00070.2008.-Chronic intermittent hypoxia (CIH) contributes to the development of hypertension in patients with obstructive sleep apnea and animal models. However, the early cardiovascular changes that precede CIH-induced hypertension are not completely understood. Nevertheless, it has been proposed that one of the possible contributing mechanisms to CIH-induced hypertension is a potentiation of carotid body (CB) hypoxic chemoreflexes. Therefore, we studied the dynamic responses of heart rate, blood pressure, and their variabilities during acute exposure to different levels of hypoxia after CIH short-term preconditioning (4 days) in cats. In addition, we measured baroreflex sensitivity (BRS) on the control of heart rate by noninvasive techniques. To assess the relationships among these indexes and CB chemoreflexes, we also recorded CB chemosensory discharges. Our data show that short-term CIH reduced BRS, potentiated the increase in heart rate induced by acute hypoxia, and was associated with a dynamic shift of heart rate variability (HRV) spectral indexes toward the low-frequency band. In addition, we found a striking linear correlation (r ϭ 0.97) between the low-to-high frequency ratio of HRV and baseline. CB chemosensory discharges in the CIH-treated cats. Thus, our results suggest that cyclic hypoxic stimulation of the CB by short-term CIH induces subtle but clear selective alterations of HRV and BRS in normotensive cats. spectral analysis; baroreflex; carotid body AUTONOMIC DYSREGULATION HAS been linked to chronic intermittent hypoxia (CIH) in animal models (22,23) and is thought to be involved in the generation of hypertension and increased cardiovascular mortality in humans with obstructive sleep apnea (OSA) (42). Indeed, repetitive hypoxic episodes in OSA patients potentiate the cardiovascular and sympathetic responses induced by acute hypoxic stimulation of peripheral chemoreceptors (16,33,35) and impair the autonomic regulation of arterial blood pressure (29, 30) and the renin-angiotensin-aldosterone system (28).The most currently accepted model for CIH-induced hypertension portrays carotid body (CB) chemoreceptor activation as one of the important mechanisms of ventilatory and cardiovascular potentiation to acute hypoxia (33). In fact, the cardioventilatory response to acute hypoxia in man and mammals is almost completely dependent on CB chemoreflexes(10, 15). Recently, Peng et al. (41) found that CIH increases the chemosensory responses of the rat CB to acute hypoxia. In the same line, we studied the early effects of CIH on cat chemosensory responses to acute hypoxia and found that cats exposed to CIH for 4 days showed enhanced CB chemosensory and ventilatory responses to acute hypoxia (43). However, the CB-medi...

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Role of vagal feedback from the lung in hypoxic-induced tachycardia in humans

Cited by 26 publications

References 0 publications

Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Dynamic time-varying analysis of heart rate and blood pressure variability in cats exposed to short-term chronic intermittent hypoxia

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